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. Author manuscript; available in PMC: 2019 Nov 1.
Published in final edited form as: J Invest Dermatol. 2018 May 9;138(11):2470–2479. doi: 10.1016/j.jid.2018.04.024

Figure 4. Dsg2 enhances epidermal and dermal uPAR in wounded tissues.

Figure 4

(a) Wild-type and K14-Dsg2 transgenic mouse epidermis (N=3) was immunoblotted for uPAR and actin. Signals were quantified, normalized to actin, and expressed as % of wild-type (right). G-uPAR: glycosylated uPAR; uPAR: non-glycosylated uPAR; uPARD2D3: D2D3 domains of uPAR. (b) Wild-type and K14-Dsg2 transgenic mice skins were immunostained for uPAR. (c) HaCaT+GFP or +Dsg2/GFP were treated with 1μg/mL anti-uPAR antibody and allowed to migrate for 24 h following scratch. Data are normalized to initial wound width of respective conditions and expressed as % distance remaining to be re-epithelialized. N=3. (d) Wild-type and K14-Dsg2 wounds (day 1) were immunostained for Laminin-332. Dashed line: regenerating basement membrane. Scale bars=50 μm.